Fluid Exchange & Edema PDF
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RAK Medical & Health Sciences University
Prof. Tarig H Merghani
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Summary
This document is a presentation on fluid exchange between plasma and the interstitium, focusing on the causes, mechanisms and types of edema. It discusses the factors affecting fluid balance and the implications of disruptions in this balance. It provides insights into the physiological issues impacting fluid exchange and edema.
Full Transcript
Fluid Exchange & Edema PROF. TARIG H MERGHANI Learning Outcomes Explain the mechanisms controlling fluid movement between the plasma and interstitial fluid, Analyze factors that contribute to the development of edema, focusing on changes in Starling’s forces. Fluid exchang...
Fluid Exchange & Edema PROF. TARIG H MERGHANI Learning Outcomes Explain the mechanisms controlling fluid movement between the plasma and interstitial fluid, Analyze factors that contribute to the development of edema, focusing on changes in Starling’s forces. Fluid exchange Between Plasma & Interstitium Occurs at the capillaries Due to two types of pressure (Starling Forces): Hydrostatic pressure (pressure of water on the vessel wall) Oncotic pressure (osmotic pressure of protein) - Mainly albumin Fluid exchange Between Plasma & Interstitium The capillaries have two pressures: Capillary hydrostatic pressure (HPc, for filtration of fluid to outside)= 10-35mmHg Capillaryoncotic pressure (πC, for absorption of fluid)= 25 mmHg Fluid exchange Between Plasma & Interstitium The ISF has two pressures: ISF hydrostatic pressure (HPISF, against filtration from capillaries) oncotic pressure (πISF, against ISF absorption into capillaries) Fluid exchange Between Plasma & Interstitium Therefore, the forces that control fluid exchange between ISF and plasma in capillaries are four (known as Starling forces). Net Filtration Pressure (NFP) NFP= HPc - HPISF - πc + πISF Fluid exchange Between Plasma & Interstitium ISF pressures are usually of low magnitude and antagonize each other; so, they are usually ignored. Net Filtration Pressure (NFP) o At the arteriolar end= (35-25) = +10 mmHg (i.e., net filtration) o At the veniolar end= (15-25) = -10 mmHg (i.e., net absorption) At the arterial end of capillaries: The capillary hydrostatic pressure > oncotic pressure resulting in filtration of fluid At the venous end of capillaries: The oncotic pressure < hydrostatic pressure resulting in absorption of 90% of filtered fluid At the venous end of capillaries: The remaining 10% of filtered fluid is absorbed by the lymphatic vessels Edema Defined as abnormal collection of fluid in the interstitium Mechanisms of edema 1- High HPc Caused by: Heart failure Venous obstruction (Deep vein thrombosis) Mechanisms of edema 2- Low OPc Caused by: Malnutrition Malabsorption Chronic liver disease Chronic renal disease (nephrotic syndrome) Mechanisms of edema 3- Lymphatic obstruction Caused by: Filariasis (elephantiasis) Tumors Surgical removal Mechanisms of edema 4- Increased permeability of capillaries to protein Caused by: Allergy Inflammation Burn Types of edema Pitting and non pitting Pitting edema All causes of High HPc and low OPc Non-pitting edema All causes of lymphatic obstruction and increased permeability of capillaries to protein Types of edema Generalized and localized Generalized edema All causes of low capillary oncotic pressure Congestive Heart failure Localized edema Lymphatic obstruction Venous obstruction Localized causes of increased permeability